Studies elucidating the behavior of HDL2 and HDL3 indicate that the A apoproteins of the subfractions of HDL are in rapid equilibrium, and are catabolized at a similar rate in the plasma. HDL apoprotein metabolism studies show that apoprotein A-I and apoprotein A-II readily associate with HDL when injected into normal subjects and subsequently are catabolized at the same rate as HDL. Apoprotein A-I and A-II studies performed in hyperchylomicronemic subjects and patients with Tangier disease, demonstrated increased catabolism. Investigations into the effect of estrogens on plasma iipoproteins indicate that estrogen administration causes increases in VLDL and HDL2 due to increased synthesis of these lipoproteins. Simultaneous 125I VLDL and 131I LDL studies in patients with homozygous familial hypercholesterolemia (FH) show that these patients have both increased production as well as defective catabolism of LDL B protein. In addition, a significant fraction of apoB appears to enter the circulation with either IDL or LDL. BIBLIOGRAPHIC REFERENCES: Schaefer, E.J.,Levy, R.I., Jenkins, L.L., Brewer,H.B., Jr.: The effects of estrogen administration on human lipoprotein metabolism. Sixth International Symposium on Drugs Affecting Lipid Metabolism, Philadelphia, 1977, in press. Phair, R.D., Hall, M., Bilheimer, D.W., Levy, R.I., Goebel, R.H., and Berman, M.: Modeling lipoprotein metabolism in man. In Proceeding of the 1976 Summer Computer Simulation Conference. Simulation Councils Inc., La Jolla, 1976, pp 486-492.